Glioblastoma multiforme (GBM) is the most common and most deadly primary brain tumor affecting adults. Despite advancements made in surgical, radiological, and chemo-therapies for this grade IV astrocytoma, prognoses have remained very poor: median survival time from diagnosis remains at 9-15 months with less than 10% of patients surviving beyond 5 years.1, 2 Caveolin-1 (Cav-1) is the principle structural protein responsible for the formation of caveolae, or invaginating microdomains in the cell membrane. The capacity for Cav-1 to associate with a wide variety of proteins has implicated it in a number of processes ranging from vesicular transport and cholesterol homeostasis to nitric oxide production and cell migration, among others.3-7 Its ability to regulate cell cycle progression and intracellular signal transduction have resulted in the substantial characterization of Cav-1 in many cancers, where it has been shown to act as both a tumor suppressor and tumor promoter depending on the tissue type.8-11 In gliomas, expression of Cav-1 appears to increase proportionally to tumor grade, with most GBM lesions exhibiting more intense Cav-1 immunoreactivity than their grade II and III counterparts. 12-14 However, little is currently known as to the role of Cav-1 as it relates to GBM in vivo. Recent in vitro studies conducted using the GBM-derived cell line U-87MG have demonstrated that Cav-1 acts as a putative tumor suppressor in GBM by downregulating α5β1 integrin expression and subsequent TGFβ/SMAD pathway activity.15 16 